Premium
[O1‐03‐08]: Amyloid imaging with Pittsburgh Compound‐B in late‐life depression
Author(s) -
Meltzer Carolyn C.,
Butters Meryl A.,
Klunk William E.,
Mathis Chester A.,
Price Julie C.,
Lopresti Brian J.,
Reynolds Charles F.,
DeKosky Stephen T.
Publication year - 2005
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2005.06.299
Subject(s) - pittsburgh compound b , late life depression , precuneus , posterior cingulate , dementia , psychology , depression (economics) , neuroimaging , magnetic resonance imaging , medicine , postmortem studies , neuroscience , cardiology , cortex (anatomy) , cognition , disease , radiology , economics , macroeconomics
online arterial sampling and 9 AD patients and 9 controls had CPK11195 PET. Spectral analysis was used to generate parametric maps of regional cerebral C-PIB binding. Compartmental analysis was used to generate parametric maps of regional brain C-PK11195 binding, a nonspecific tissue reference input function being defined with cluster analysis. Object maps were created by segmenting individual MRIs and spatially transforming the grey matter images and PET scans into standard stereotaxic MNI space on which a probabilistic atlas was superimposed. Significant clusters of increased C-PIB and C-PK11195 binding in AD were localised with SPM99 software. A correlation coefficient map was then generated from the coregistered Alzheimer PK and PIB scans with SSM software. Results: PIB-SPM PK-SPM Correlation map C-PIB PET showed significant 2-3 fold increases in amyloid load in the frontal, temporal, parietal, occipital association cortex of AD patients (p 0.0001) [Fig1]. C-PK11195 PET detected an increase in frontal, temporal, parietaletal, and occipital microglial activation in AD (p 0.05) [Fig2]. The correlation map shows voxels where there are parallel increases in C-PIB and C-PK11195 uptake (p 0.05, r 0.68)[Fig3] in 7 AD patients who had both scans. Conclusion: Increased amyloid load in cortical association areas in Alzheimer’s disease positively correlates with the presence of increased microglial activation. This provides a rationale for examining both these pathologies when studying the efficacy of putative anti-amyloid agents.